Li C Y, Li Z W
Research Centre of Experimental Medicine, Tongji Medical University.
Sheng Li Xue Bao. 1990 Oct;42(5):437-45.
Intracellular recordings were made to investigate the effect of acetylcholine (ACh) on membrane potential of neurons in isolated toad dorsal root ganglion (DRG). In the 73 neurons examined, 67 were of type A, and the remaining 6 of type C cell. The resting membrane potential of these two types of cells was -67.5 +/- 1.3 mV (mean +/- SE). During the application of ACh (4 x 10(-4)-6 x 10(-4) mol/L) four types of the membrane potential changes were observed: (1) hyperpolarization of 9.1 +/- 3.0 mV (mean +/- SE, n = 23); (2) depolarization of 12.9 +/- 2.2 mV (mean +/- SE, n = 20); (3) biphasic response, i.e., hyperpolarization of 8.0 +/- 2.4 mV (mean +/- SE) followed by depolarization of 10.9 +/- 3.1 mV (mean +/- SE, n = 24); (4) no change (n = 6). The hyperpolarization induced by ACh could be blocked by atropine (1.3 x 10(-5) mol/L, n = 23), and ACh-induced depolarization could be abolished by coperfusion of d-tubocurarine (1.4 x 10(-5) mol/L) and hexamethonium (1.4 x 10(-5) mol/L, n = 18). During ACh hyperpolarization the membrane conductance was increased by 13.8% and the reversal potential was about -96 mV (n = 3). TEA (20 mmol/L) enhanced ACh depolarization amplitude by 48.2 +/- 3.2% (mean +/- SE, n = 6), and depressed ACh hyperpolarization by 79.4 +/- 4.3% (mean +/- SE, n = 8), MnCl2 (4 mmol/L) decreased the ACh depolarization and hyperpolarization by 54.2 +/- 7.2% (mean +/- SE, n = 5) and by 69.2 +/- 6.4% (mean +/- SE, n = 14) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)